4-Acetylantroquinonol B suppresses autophagic flux and improves cisplatin sensitivity in highly aggressive epithelial cancer through the PI3K/Akt/mTOR/p70S6K signaling pathway

Liu, Mingche; Bamodu, Oluwaseun Adebayo; Huang, Wen Chien; Zucha, Muhammad Ary; Lin, Yen Kuang; Wu, Alexander T.H.; Huang, Chun Chih; Lee, Wei Hwa; Yuan, Chiou‐Chung; Hsiao, Michael; Deng, Li; Tzeng, Yew Min; Yeh, Chi Tai

doi:10.1016/j.taap.2017.04.003

Cited by 41 publications

(33 citation statements)

References 40 publications

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“…In previous researches, a large amount of evidence proved that cisplatin acted as an autophagy stimulator in cancers. For instance, it had been verified to cause cell autophagy in ovarian cancer, 45 bladder cancer 46 and malignant mesothelioma. 47 While in this study, we proved that cisplatin could also induce autophagy in ATC cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation

Liu

Feng

Zhang

et al. 2018

Cancer Biology & Therapy

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Section: Discussionmentioning

confidence: 99%

Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation

Liu

Feng

Zhang

et al. 2018

Cancer Biology & Therapy

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“…6 Autophagic cell death is an alternative form of programmed cell death that is distinct from apoptosis and that has been observed in the context of PC. 6,26 Autophagy is associated with a disruption of apoptotic induction, whereas caspase activity that is induced during apoptosis can, in turn, disrupt autophagic processes. In some contexts, however, autophagy and related signaling processes can trigger tumor regression and cell death.…”

Section: Discussionmentioning

confidence: 99%

“…In some contexts, however, autophagy and related signaling processes can trigger tumor regression and cell death. 26 The speci c mechanisms governing autophagy are highly complex and tightly regulated.…”

Section: Discussionmentioning

confidence: 99%

“…The PI3K-Akt-mTOR signaling pathway is associated with autophagic activity, and controls the differentiation, survival, proliferation, and migration of cells. 26 Akt functions as the primary mediator of PI3K signaling, with mTOR being a downstream target of this PI3K/Akt signaling pathway. 7,9 mTOR functionality is primarily governed by the activity of two different complexes (mTOR1 and mTORC2), with mTORC1 kinase activity serving to suppress autophagy and to maintain homeostatic cell growth, proliferation, and survival.…”

Section: Discussionmentioning

confidence: 99%

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The impact of Icariside II on human prostate cancer cell proliferation, mobility, and autophagy via PI3K-AKT-mTOR signaling pathway

Zhan

Xie

et al. 2020

Preprint

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Background The flavonol glycoside icariside Ⅱ (ICA II) has been shown to exhibit a range of anti-tumor properties. Herein we evaluated the impact of ICA II on the proliferation, motility, and autophagy activity of human prostate cancer cells, and we further evaluated the molecular mechanisms underlying these effects. Methods Herein, we treated DU145 human prostate cancer cells with a range of ICA II doses. We then evaluated the proliferative abilities of these cells via CCK-8 assay, whereas apoptosis and cell cycle status were assessed via flow cytometry. We further utilized wound healing and transwell assays to probe the impact of ICA II on migratory and invasive activities, while autophagy was assessed via laser confocal fluorescence microscopy. Western blotting was further utilized to measure LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K levels, with RT-PCR being used to evaluate the expression of these same genes at the mRNA level. Results We found that ICA II was capable of mediating a dose- and time-dependent suppression of prostate cancer cell proliferative activity, while also causing these cells to enter a state of cell cycle arrest and apoptosis. We further determined that ICA II treatment was associated with significant impairment of prostate cancer cell migratory and invasive abilities, whereas autophagy was enhanced in treated cells relative to untreated controls. Levels of p-P70S6K, p-mTOR, p-AKT, and PI3K were all also decreased by ICA II. Conclusion Our results indicate that ICA II treatment is capable of suppressing human prostate tumor cell proliferation and disrupting migratory activity while enhancing autophagy through PI3K-AKT-mTOR signaling. As such, ICA II may be an ideal candidate drug for the treatment of prostate cancer.

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“…As an important signal transduction pathway, PI3K-Akt-mTOR is involved in many cellular processes, including cell apoptosis, survival and proliferation (Liu et al 2017). Phosphatidylinositol 3 kinase (PI3K) is an intracellular phosphatidylinositol kinase (Hennessy et al 2005).…”

Section: Introductionmentioning

confidence: 99%

A preliminary report: genistein attenuates cerebral ischemia injury in ovariectomized rats via regulation of the PI3K-Akt-mTOR pathway

Lu¹,

Liu²,

Gong³

et al. 2019

gpb

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Stroke is a leading cause of disability and death in the worldwide. Therefore, prevention of stroke is critically important. Genistein, a natural phytoestrogen extracted from soybeans, has been found to be a potential neuroprotective agent for stroke prevention. However, the role of genistein and its underlying mechanism in ovariectomized rats has been rarely evaluated. In this study, ovariectomized rats were treated with genistein (10 mg/kg) or vehicle daily for two weeks before they received middle cerebral artery occlusion (MCAO) and reperfusion. Seventy-two hours after reperfusion, the neurological function was evaluated by Garcia test, infarct volumes were detected by 2,3,5-triphenyltetrazolium chloride staining; and neuronal damage and cell apoptosis were detected by Nissl and Tunel staining in the ischemic penumbra, respectively. In addition, Western blotting was used to detect the activity of PI3K-Akt-mTOR signal pathway in the ischemic penumbra in different groups. And we found that genistein treatment in ovariectomized rats significantly improved neurological outcomes, reduced infarct volumes, decreased neuronal damage and cell apoptosis, and increased the activity of PI3K-Akt-mTOR signal pathway. Our findings indicated that treatment genistein could alleviate neuronal apoptosis induced by cerebral ischemia in ovariectomized rats via promoting the activity of PI3K-Akt-mTOR signal pathway, which provides a new molecular mechanism for the neuroprotective effects of genistein against stroke.

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4-Acetylantroquinonol B suppresses autophagic flux and improves cisplatin sensitivity in highly aggressive epithelial cancer through the PI3K/Akt/mTOR/p70S6K signaling pathway

Cited by 41 publications

References 40 publications

Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation

Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation

The impact of Icariside II on human prostate cancer cell proliferation, mobility, and autophagy via PI3K-AKT-mTOR signaling pathway

A preliminary report: genistein attenuates cerebral ischemia injury in ovariectomized rats via regulation of the PI3K-Akt-mTOR pathway

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